acute Inflammation Flashcards

1
Q

What are the signs of acute inflammation

A

Heat
Redness
Swelling
Pain
Loss of function

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

Define acute inflammation

A

Redundant, complex, adaptive & protective response of vessels, resident cells & leucocytes to noxious stimuli

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

How does acute inflammation work?

A

Inflammation brings cells & molecules of host defence from circulation to sites where they are needed, in order to eliminate offending agents & repair tissues

Lasts hours to days

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

Give examples of causes of acute inflammation

A

Infections (bacterial, fungal, viral, parasitic) & microbial toxins

Tissue necrosis, ischemia, trauma, physical & chemical injury, irradiation

Foreign bodies

Immune reactions

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

What are the morphologic hallmarks of acute inflammation?

A

Dilation of blood vessels

Activation & recruitment of leucocytes

Active exudation of fluid in extravascular tissue

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

What are the mediators in acute inflammation & where are they produced?

A

Vasoactive amines (histamine, serotonine)
- released/produced by mast cells, basophils, platelets

Inflammatory lipids (prostaglandins, leukotrienes)
- produced by mast cells, leukocytes

Complement (C5a, C3a)
- produced in liver

Cytokines (IL-1, TNF, IL-6)
- produced by macrophages, endothelial cells, mast cells

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

Which inflammatory mediators cause vasodilation in acute inflammation?

A

Inflammatory lipids (prostaglandins, leukotrienes)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

Which inflammatory mediators cause increased vascular permeability in acute inflammation?

A

Vasoactive amines

Complement (C5a, C3a)

Inflammatory lipids

Cytokines (IL-1, TNF)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

Which inflammatory mediators cause leukocyte recruitment & activation in acute inflammation?

A

Inflammatory lipids

Complement

Cytokines

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

Which inflammatory mediators cause pain in acute inflammation?

A

Inflammatory lipids

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

Which inflammatory mediators cause tissue damage in acute inflammation?

A

Release of neutrophilic cytoplasmic granular content (enzymes)

Reactive oxygen species (produced by neutrophils & leukocytes)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

What are the possible consequences of acute inflammation

A

Complete resolution

Scarring or fibrosis

Progression to chronic inflammation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

describe complete resolution as an outcome of acute inflammation

A

Complete resolution happens when:
- injury is limited in extent
- There is minimal tissue destruction & damaged parenchymal cells can regenerate

This leads to clearance of offending agent & full tissue regeneration

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

describe scarring/fibrosis as an outcome of acute inflammation

A

Scarring (fibrosis) occurs when:
- There is substantial tissue destruction
- inflammatory injury affects tissues incapable of regeneration
- Fibrin exudation in tissues or serous cavities (pleura, peritoneum) can’t be cleared

In these cases, connective tissue replaces damaged area, forming mass of fibrous tissue

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

describe progression to chronic inflammation as an outcome of acute inflammation

A

Acute inflammation becomes chronic when:
- injurious agent persists
- There is interference in normal healing

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

Describe acute phase response in acute inflammation

A

systemic reaction to acute inflammation, involving:
- Pyrexia (fever)
- Leukocytosis (increased WBC count)
- Metabolic changes
- Changes in plasma proteins (acute phase proteins, APPs)

17
Q

How is acute inflammation similar to a dripping tap?

A

Leakage of inflammatory cytokines acts both locally & systemically

This “dripping effect” triggers widespread systemic changes

Continuous release of inflammatory mediators leads to acute phase response

18
Q

What causes pyrexia?

A

Fever is caused by increase in hypothalamic set point, leading to elevated core body temp

Fever is triggered by exogenous or endogenous pyrogens, which activate host immune response

19
Q

Describe the pyrexia pathway

A
  1. Exogenous pyrogens (e.g. bacteria) & endogenous triggers (e.g. phagocytosis, tissue damage, immune complexes) stimulate:
  2. Neutrophils & Macrophages, which release:
  3. Endogenous pyrogens (IL-1, TNF, IL-6), leading to:
  4. Increased production of PGE₂ (Prostaglandin E₂), which acts on:
  5. Hypothalamus, increasing body temp via vasoconstriction & shivering
20
Q

How can pyrexia be regulated?

A

NSAIDs act as antipyretics by inhibiting PGE₂ synthesis, reducing fever

21
Q

What is a biomarker?

A

biological molecule that is objectively measured & is indicator of normal or abnormal process, or of a condition or disease

22
Q

What are the positive APP biomarkers of inflammation?

A
23
Q

What are the negative APP biomarkers of inflammation?

A
24
Q

What are the types of exudate in acute inflammation?

A
25
Q

What is transudate in acute inflammation?

A

Extravascular filtrate of protein & cell poor fluid

Caused by increased hydrostatic pressure or due to decreased colloido-osmotic pressure (or combination)

It is accumulated in body cavities & extracellular compartments

Fluid appears grossly clear & watery